A Blood Test That Could Diagnose Alzheimer's Shows Promise.

In what might prove to be an important advance in getting treatment to Alzheimer's patients as early as possible, UCLA researchers have found that a simple blood test might be developed that could diagnose patients with Alzheimer's.

While there is currently no cure for Alzheimer's, getting treatment to patients as early as possible is important, as many treatments are most effective in the earliest stages of the disease.

At present, the only way to definitely prove the presence of Alzheimer’s is through the examination of brain tissue after death, however, to diagnose patients while they are alive, doctors rely on the presence of biomarkers (beta amyloid proteins in the brain, a hallmark of the disease) and cognitive symptoms such as memory loss.

Two methods are currently used to determine the beta-amyloid formation characteristic of Alzheimer’s disease, however, there are significant drawbacks to both. A spinal tap can be used to obtain cerebrospinal fluid, however, this is an invasive procedure that carries the risk of nerve damage and other serious side effects. Alternatively, an amyloid PET scan can be used, and while this technology is non-invasive, it exposes subjects to radiation. Moreover, amyloid PET scans are available in only few medical centers, and are not typically covered by insurance as a diagnostic test. 

For their study, the UCLA researchers developed a simple signature for predicting the presence of brain amyloidosis — the build-up of amyloid in the brain — including several blood proteins known to be associated with Alzheimer’s disease, along with information routinely obtained in the course of a clinical work-up for patients suspected to have the disease, such as results of memory testing and structural magnetic resonance imaging.

The UCLA researchers found that their method could be used to predict the presence of amyloid in the brain with modest accuracy.

"Our study suggests that blood protein panels can be used to establish the presence of Alzheimer’s-type pathology of the brain in a safe and minimally invasive manner,” said Liana Apostolova, MD, director of the neuroimaging laboratory at the Mary S. Easton Center for Alzheimer’s Disease Research at UCLA and head of the research team. “We need to further refine and improve on the power of this signature by introducing new disease-related metrics, but this indicates that such a test is feasible and could be on the market before long.”

Results of the study appeared in the journal Neurology.

A Non-Drug Therapy May Show Promise

Axona® is a new, prescription dietary supplement (non-drug therapy) designed to support cognition and memory in individuals with Alzheimer's.

Axona is not a replacement for drug therapies that target the chemicals that brain cells need to function, instead, Axona addresses another factor influencing reduced cognition—diminished cerebral glucose metabolism (DCGM).  

To function properly, the brain needs too consume a lot of fuel, in the form of a constant supply of glucose (a kind of sugar). When glucose levels are too low, brain cells do not function properly and memory and other cognitive processes are affected.

Research has shown that Alzheimer's interferes with the brain's ability to process and use glucose. This is called diminished cerebral glucose metabolism (DCGM).

However, when glucose levels are too low, the body produces a back-up source of nutrition for the brain know as ketone bodies. Ketone bodies are naturally produced by the liver. 

Axona contains fatty acids called medium-chain triglycerides (MCTs), which the body converts into ketone bodies to help support cognition in patients with mild-to-moderate Alzheimer's disease.

Clinical studies have shown that raised ketone body levels can enhance memory and cognition in some people with mild to moderate Alzheimer’s disease.

The John Douglas French Alzheimer's Foundation is funding a study at UCLA examining the cerebral metabolic effects of AC-1202 (Axona®) treatment in mild-to-moderate Alzheimer’s disease (AD), using positron emission tomography (PET). Subjects in the study include both carriers and non-carriers of the APOE4 gene.

The John Douglas French Alzheimer's Foundation also funded an initial study of ketone ester in Alzheimer's disease in mice, conducted by Dr. Richard Veech and Dr Yoshihiro Kashiwaya at the NIH. The study found that feeding the ketone ester to mice (1) decreased amyloid accumulation in brain, (2) decreased phosphorylated tau and (3) improved cognitive performance in the mice.

Learn more about Axona by visiting the Axona website HERE and reading a report on Axona by the Mayo Clinic HERE

A tough question for parents: Considering the risks for brain damage, should you let your son play football?

In recent years there has been increasing awareness of the long-term effects of brain trauma.  Recent studies have confirmed that a history of at least one mild-traumatic brain injury increases the likelihood of dementia later in life.  

Trauma appears to predispose to not only Alzheimer’s disease, but also Parkinson’s disease and Lou Gehrig’s disease (amyotrophic lateral sclerosis).  Individuals who suffer from multiple traumatic injuries are particularly vulnerable to a disorder that has been called Chronic Traumatic Encephalopathy or CTE.  

This syndrome has also been described in wrestlers, boxers, war veterans and altheletes involved in contact sports. CTE  begins as a behavioral disorder with anxiety, anger, disinhibition, and sometimes problems with memory or multi-tasking and is followed by the development of motor problems, dementia and eventually death.  The brain shows the pathological accumulation of the tau protein and sometimes a protein called TDP-43.  No treatments exist yet for CTE, but avoiding head trauma is the best way to avoid this devastating disorder.

With that in mind, parents should carefully consider the risks for long-term brain damage when deciding whether or not to let their sons play football.

Dr. Bruce Miller, Director of the UCSF Memory and Aging Center and Chief Medical Officer of The John Douglas French Alzheimer's Foundation, heads a team involved in a study analyzing head impacts incurred by NFL players and the part it may play in future dementia.

After decades of dead-ends and frustration, researchers are finally looking in a new direction for the cause of Alzheimer's.

A new study by the Mayo Clinic published in Brain, points to Tau Protein—not Amyloid (the agent long thought to be the cause of Alzheimer's) as the primary driver of the disease.

For more than a decade, JDFAF's Chief Medical Officer, Bruce Miller, MD has been a pioneer in exploring Tau as the cause of Alzheimer's.  Dr. Miller who heads the UCSF Memory and Aging Center is also a founder of the Tau Consortium, an international group of clinical and basic scientists who work together with a sense of urgency to understand, treat, and cure tau-related disorders.

In the new study, researchers at Mayo Clinic’s campuses in Jacksonville, Florida, and Rochester, Minnesota studied 3,600 postmortem brains and found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer’s disease, not Amyloid, as previously thought.  Amyloid is another toxic protein that characterizes Alzheimer’s which builds-up as dementia progresses, but the researchers have concluded that it is not the primary cause.

“The majority of the Alzheimer’s research field has really focused on amyloid over the last 25 years,” says Melissa Murray, PhD, the chief investigator of the study. “Initially, patients who were discovered to have mutations or changes in the amyloid gene were found to have severe Alzheimer’s pathology — particularly in increased levels of amyloid. Brain scans performed over the last decade revealed that amyloid accumulated as people progressed, so most Alzheimer’s models were based on amyloid toxicity. In this way, the Alzheimer’s field became myopic.”

Based on the study, Dr. Murray concludes that halting toxic tau should be a new focus for Alzheimer’s treatment.

Read the full report on the Mayo Clinic Website.